LEAD AND PREGNANCY
Maternalversus cord blood and foetal blood lead levels50 are highly correlated, r = 0.80 and 0.81 respectively. Excessive lead exposure during pregnancy has been found to give rise to neurological damage to infants, to intrauterine and postnatal growth retardation,51 and to a high proportion of retarded infants.52 Subtoxic material levels are associated with an increased risk of premature delivery,53 miscarriage,12 and reduction in birth weight54 and raised placental lead levels have been shown to give rise to stillbirths and congenital. abnormalities. 55 Although inconclusive evidence was found by one group of researchers trying to link low maternal blood and cord blood lead levels with deformities,49 maternal levels down to 10 ug/dl (but not postnatal exposure) have been found by others to retard development from 6 months to 2 years of age.56 Hence the foetus is probably affected by lead levels well below 20 ug/dl. Lead concentrations of around 40 p.p.m. have been found in the bones of stillborn infants. 12 At 2 p.p.m of lead birth is normal. The question has been asked: What are the affects on the foetus of lead exposure which causes a concentration in bone of, say, 20 p.p.m. ? Such exposure postnatally would not be recognised as being dangerous. However, such exposure may be dangerous to the foetus, the effects appearing later in life, untreatable, and the connection with lead exposure going unrecognised.
IS THERE REALLY A SAFETY LIMIT?
In recent years, the safety limit of lead in blood has been gradually reduced and the evidence is. that it should be reduced still further below the now acceptable level of 20 ug/dl especially as children are more sensitive to lead than adults and the foetus most probably even more so. Is there, in fact, a safe limit at all? - a level below which lead has no effect - a threshold, or conversely, a continuum?. Early signs and symptoms of lead toxicity are vague and non- specific: abdominal pain, loss of appetite, headache, listlessness, vague personality changes etc. They are usually not associated in the clinician’s mind with lead toxicity, and lead levels are rarely measured at this stage, until the disease has progressed to an acute or nearly catastrophic encephalopathic incident. Hence, a continuum of illness43 prevails from the non-specific CNS symptomatology to the acutely dramatic catastrophe. The generally accepted. threshold view thus does not apply. In starting at the vague non-specific end of the spectrum and considering chronic cases of lower and lower blood lead level, CNS symptomatology - learning disability, mental.retardation, hyperactivity, perceptual motor disability, conduct disturbances etc. becomes more and more vague, but is there a threshold below which there is no effect? Although there seems to be a threshold level of 11.5 ug/dl above which the age at which children first sit up or speak is increased, the age at which children first start walking seems to be affected at lower and lower levels on investigation,57 1.0. differences at 14.4 and 11.4 ug/dl have been found,27 the elevation of hearing thresholds in young people continue down to at least 5 ug/dl57 and growth in children is certainly affected down to 4 ug/dl.58 These authors,57,58 show statistically that these last two factors should be influenced at still lower levels of lead, theoretically down to zero and it thus appears that there is a continuum: no true safe Level i.e. any lead level has an effect. Blood lead levels in ancient man were estimated to be around 0.2 ug/dl and in the remote Yanomama Indians a mean level of 0.83 ug/dl was found. Even in the Himalayan foothills of Nepal a mean level of 3.4 ug/dl was found in the population and it seems that global pollution is almost so complete that mankind is living at 10-200 times the norm for lead or even more.
BLOOD LEAD: SOURCE AND FACTORS
The main sources are environmental, occupational and, in Pakistan, cosmetical; important factors are nutritional status and socioeconomic factors. Apart from contamination of the water supply and fish and other food sources by industrial effluents and of land and vegetables by the use of sewage sludge as fertilizer, the use of leaded petrol and of lead paints, solders, pipes etc. and contamination by certain industries of their surroundings, must, in general, be the most important environmental sources of lead in the body. Evidence for the importance of lead emitted in the exhaust of petrol driven vehicles is legion, for example, trainers for a marathon in South Africa in rural areas had levels 4.2-42.8 (mean 20.1 ug/dl) and in urban areas 19.9-77.7 (51.9) whereas controls in remote areas had 3.0- 16.0 (9.7): Competitors pre-race bad 25-93(45.8) and afterwards 25-105(53 ug/dl). 60 Blood lead levels as high as 97 ug/dl were reported in traffic constables in Alexandria, Egypt.61 Between 1976 and 1980, a drop of 36.7% in the mean blood lead level was reported in U.S.A. due mainly to the introduction of lead free petrol2 Since the clean up of local industries, the abandonment of lead based paints and varnishes and the replacement of lead-soldered food and drinks cans by seamless welded containers, mean blood lead levels fell by 42-46% in Christchurch, New Zealand although petrol and water consumption remained approximately constant and the lead content of both did not vary. 62 Workers and theft families in the lead industry are at risk. For example, levels of up to 280 ug/dl were reported in workers at a lead smelting plant in U.S.A.,24 amongst whom some had G.I.t problems, extensor muscle weakness (at above 40 ug/dl) and anaemia (above 60 ug/dl) and all with levels of 35 ug/dl upwards and a minimum of seven years exposure had renal problems. The homes of workers exposed to lead borosilicate dust at a capacitor factory in U.S.A. were contaminated with more lead and the children had higher blood lead levels, than those of unexposed workers, due to the dust carried home on clothing. 40 Surma in Pakistan, which in the past contained antimony, now contains up to 89% lead as lead sulphide. Its use has recently been reported (1988) as being responsible for causing blood lead levels of up to 80 ug/ dl. Fortunately there appeared to be no clinical ill- effects63 as was reported earlier among a group of surma-using Punjabi immigrants in U.K., who were using material obtained mostly from abroad. Levels of up to 70 ug/dl were found. 64 However, death due to encephalopathy of a surma user has been reported in U.K. 65 Clearly, its use should be forbidden bylaw. Nutritional deficiencies of iron, zinc, copper, calcium and phosphorus enhance the absorption of lead from the diet. 66 Lead absorption is higher in iron deficiency anaemia in humans67 and also in protein deficiency in rats. 68 A high lead diet in rats produces copper deficiency, 69 and lead in humans competes with zinc, iron, and calcium and thus interferes with embryonic nutrition. 70 Childhood exposure to lead in general is higher in low income areas owing to the environment, peeling paint in houses etc., and to deficiencies in child care and household cleanliness71 Neurological effects of such exposure are also greater. 72 One can assume that nutritional factors are at least partly the cause and that these facts apply to adults in socially disadvantaged groups also. Increased blood lead levels have been found in smokers, probably lead is present in the tobacco. 73 Alcohol intake results in higher blood lead levels especially among wine drinkers and it has been found that the lead content of wines is greater than that of spirits or beers. 74 Those with liver disease without cirrhosis had higher levels than cirrhotics. 74 Possibly lead accumulates in the livers of cirrbotics and acute liver damage induced by alcohol releases the lead.75
RACIAL AND INDWIDUAL VARIATIONS IN THE EFFECTS OF LEAD
A series of studies has been carried out in various population groups in Karachi and blood lead levels, mostly, are alarmingly high. The obvious question is why is the incidence of neurological disease not higher even than it is? Admittedly, a blood lead level is not a good indicator of lead status, for reasons mentioned earlier, but short of going around doing brain biopsies ad lib., there is no other satisfactory method, as enzqme estimations are even less reliable indicators. 7,8 Could the effects of lead be less serious than among Westerners? Many differences in biochemistry occur between Pakistanis and Westerners as differences in normal ranges indicate. It cannot yet be known if this applies to the effects of lead but certainly American negroes are less affected than white Americans, hence a racial difference. Although higher blood lead levels are found among black American children than among white, 48,76,77 the former have better hearing abilities than the latter76 and they develop quicker during the first year of life.77 (Lead is detrimental to both these factors57,58). Individuals vary greatly in their response to lead. A blood lead level of 100 ug/dl can literally kill one person and have no effect on another. 42 A worker at a lead smeltings plant in U.S.A. bad a lead level of 280 ug/dI which was toxic but not fatal24 At a levels 48.4-95.4 ug/dl yet only 50% suffered from insomnia, 44.6% with fatigue, 41.4% with abdominal colic, 37.6% with weakness, 29.0% with drowsiness and 2% only had a blue gum line. 78 In November1988 it was reported from U.K. concerning evidence for the existence of, what has simply been described as, a low molecular weight protein in red blood cells, which chelates with lead and supposedly prevents its toxic action. This protein was absent in those with low blood lead levels, is present in low concentration in those with high lead levels exhibiting signs of lead toxicity, and is present in higher concentration in those with high lead levels with no symptoms of lead toxicity. 79 So, perhaps, all is not doom and gloom!
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